Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
105 Cards in this Set
- Front
- Back
|
Lashleys search for Engram
|
Karl Lashley was looking for memory trace. He trained animals to do some complicated task- brightness discrimination or maze orientaion and removed part of brain either before or after, then recorded influence of lesion on memory and learning
|
|
|
Two principles discovered by Lashley
|
Mass action principle -reduction in learning is proportional to the amount of tissue destroyed, more complex task - more disruptive lesion
Equipotentiality principle - all cortical areas can substitute for each other in learning |
|
|
Lashleys conclusions
|
learning is a distributed process that could not be isolated within any particular area of the brain. Location is not important, but amount of tissue destroyed.
|
|
|
Development of scientific models
|
step one - inductive process - creating model, explanation or hypothesis
step two - deduction - testing the hypothesis step three - experimental testing of the model either to disprove it or validate |
|
|
Induction and Deduction
|
Induction - putting all facts together to create explanation of reality
Deduction - putting explanations of reality or hypotheses to test |
|
|
Sensory memory
|
lasts very brief time, from 1 to 3 seoonds, holds information in physical form (unprocessed), occurs without attention
|
|
|
Iconic memory
|
short term sensory store for vision, discovered by George Sperling, holds apparently everything seen, not limited, less then one second, was first to be discovered
|
|
|
Echoic memory
|
short term sensory store for auditory information, hold sounds in sound form, 3 to 4 seconds, thought to help a lot in understanding speech
|
|
|
Short term memory capacity
|
limited capacity, can only hold 7+- 2 items at a time, capacity can be increased by chunking (grouping)
|
|
|
Short term memory duration
|
unrehearsed information can only be held for several seconds before its forgotten. Rehearsal can extend duration indefinitely, can be overt and covert ( out loud and silent). To prevent confounding, count backwards
|
|
|
Encoding
|
stimuli arent just transported to memory, certain aspects are noticed and analyzed, others are ignored, selective process, prerequisite for remembering
|
|
|
Types of encoding
|
phonological - while rehearsing strings of letters mistakes that are made are usually phonological - v vs b
visual - explain mental rotation semantic coding - release from proactive interference |
|
|
Storage
|
process of transferring of enncoded information to memory
|
|
|
Retrieval
|
process of extracting knowledge previously stored in long term memory
|
|
|
Free recall
|
free recall - subjects asked to retrieve stimulus items from memory, original stimulus is not present during the test, items may be recalled in any order, order of item recall is due to organization in memory
|
|
|
Serial Recall
|
subjects recall items in the order presented, original stimulus is not present during test, used to reveal serial position effect
|
|
|
Cued recall
|
subjects recall items with the help of cues
categorical cues - can you remember the names of any animals on the list paired associate cues - can you remember the word that was paired with tree original stimulus not present, used to reveal serial position effect |
|
|
Why is short term memory also called working memory
|
active system for temporarily storing and manipulating information needed in execution of complex cognitive tasks - learning reasoning etc
two parts - storage and central executive |
|
|
Long term memory capacity
|
unlimited, never has been a case of LTM full to capacity
|
|
|
LTM duration
|
Unless there is an organic brain damage, unlimited, though can experience failures of retrieval
|
|
|
Interaction of LTM and working memory
|
there are primacy and recency effects
there is a better recall at the eginning of the list due to primacy effect and better recall at the end due to recency effect, worse recall in the middle due to proactive interference |
|
|
Proactive interference
|
new items interfere with subsequent items in the list
|
|
|
Two types of LTM
|
Declarative (facts) and procedural (skills)
|
|
|
Declarative memory
|
semantic - facts and general world knowledge
episodic - autobiographical, events and experiences, explicit memory - can be verbalised |
|
|
Procedural memory
|
knowing how, skills ( i.e riding a bike), implicit memory - cannot be verbalised
example - classical conditioning |
|
|
Types of amnesia
|
anterograde - poor memory for events that have happened since the onset of disease
retrograde - loss of memory for events that have happened before onset of disease |
|
|
Temporal gradient
|
older memories are better to stay
|
|
|
A patient develops an encoding deficit. He/she is unable to create new long term memory representations, preserved retrieval skills. What would you expect to see - retrograde or anterograde amnesia
|
anterograde amnesia, because encoding deficit will prevent him/her from creating any new long-term memories. There will be hardly any retrograde amnesia, unless onset of illness interferes with processes which consolidate recently acquired memories
|
|
|
A patient develops a retrieval deficit. He/she can create new long ter memories but can retrieve in recall. What would you expect to see - retrograde or anterograde amnesia?
|
both, retrieval deficit would prevent the patient recalling both recently established and long established memories
|
|
|
How could you distinguish a retrieval only deficit from a combination of an encoding and retrieval deficit
|
with great difficulty
|
|
|
Are there aspects of memory which can survive in amnesia?
|
short term memory(digit span) can be normal, semantic memory - amnesics show good comprehension of words and objects and may retain a lot of factual information
|
|
|
Memory consolidation
|
In order for a memory trace to be consolidated new proteins and RNA must be made, new proteins contribute to morphological changes (synapse lengthening or new synapse formation)that consolidate the memory trace over a long period of time
|
|
|
Traumatic brain injury
|
any injury to the head that disturbs or damages brain function, most common cause - car accidents, head is injured in more then 2/3 of car accidents, cause of death in 70% of fatal cases, third most common cause of death in USA and primary cause of death of persons under 38, 7 million per year in USA
|
|
|
Blunt Head injury
|
dura mater has not been perforated, sudden impact causes the head to twist on the neck, brain rotates inside the skull,rapid rotation causes damage to neurons, tearing of long axons, also tearing of blood vessels that results in bleeding, causes damage to brain - diffuse injury, especially brain stem and cerebellum which results in loss of consciousness, breathing and change in blood pressure (rise)
|
|
|
Coup
|
sudden impact ( head hitting an automobile dashboard), causing in addition focal injury to the frontal part of the brain ( frontal and temporal lobes)
|
|
|
Countre coup
|
brain rebounds from the below and hits the opposite side, produce bruising and bleeding to both the front and back portions of the brain, usually in boxing
|
|
|
Damage to cerebellum
|
lack of muscle control and balance
|
|
|
Damage to brainstem
|
brainstem can move as long as several centimeters inside of the head, may result in lack of consciousness, suspension of breathing, blood pressure changes
|
|
|
Lack of consciousness
|
this state may be short and prolonged (coma),injury is severe if coma lasts more then 6 hours
|
|
|
Apnea
|
suspension of breathing, respiratory centers are located in brainstem, can last for several minutes, lack of oxygen causes hypoxia, can also cause death, important to give artificial ventilation
|
|
|
Blood pressure changes
|
rapid and major rise of arterial blood pressure, can break through auto-regulation process and cause rupture of blood vessels and upset chemical balances
|
|
|
Post traumatic amnesia
|
blow to the head causes temporary amnesia, combination of encoding and retrieval deficit, retrieval deficit causes retrograde amnesia, encoding deficit causes anterograde amnesia. After recovery patient remains unable to remember anything from amnesic period
|
|
|
Recovery temporary factors
|
some head injury factors such as intracranial pressure may contribute to irreversible effects of brain trauma.
|
|
|
Regenerative and collateral sprouting
|
Regeneration - some disrupted fiber processes may grow back and establish pre injury connections
Collateral sprouting - intact neurons produce branches that occupy empty site |
|
|
Redundancy
|
There are latent (previously unused) neural connections that get activated when the brain is damaged
|
|
|
Vicarious functioning
|
neural tissues not normally involved in the performance of a task, alter properties after injury
|
|
|
Other recovery factors
|
1. age differences - young recover faster
2. task differences - simple tasks easier to do 3. enviromental effects - enriched and stimulating environment helps |
|
|
Islands of Memory
|
Memory of special events could be retained (visit from a friend), islands of memory lack temporal sequence and coherence, do not imply termination of PTA, may go on several days before PTA ends
|
|
|
Delayed PTA
|
all the details of the event retained, but then follows a period of amnesia, usually when there is little or no loss of consciousness, results from vascular complications (extradural hematoma), higher in gunshot injuries because of localized trauma and no diffuse injury
|
|
|
Paramensia
|
some patients confuse with other injury in similar setting
|
|
|
Confabulation
|
filling the gaps in memory by fabrications, that are described as actual events, usually actual experiences but altered in details and context
|
|
|
Transient global amnesia
|
a sudden onset of transient inability to retain new information and to recall previous events for a variable period of time
|
|
|
3 hypothesis of etiology of transient global amnesia
|
1. vascular hypothesis - transient ischemia of posterior cerebral artery causing dysfunction of limbic system
2. epileptic hypothesis - electrical events of hippocampus or medial temporal lobe 3.migraine hypothesis - cerebral blood flow abnormalities consistent with migraines |
|
|
Precipitating factors of TGA
|
pain, sexual intercourse, mild head trauma, highly emotional experience, angiography with contrast injection
|
|
|
Clinical TGA
|
arupt onset, lasting few hours and then disappearing, patient cant remember event, and sometimes events before onset, patients are aware of deficit, restless, anxious, asking same questions. Immediate memory retained, verbal and non verbal, personal identity, consciousness, no focal neurological signs
|
|
|
Name meninges
|
Pia mater, arachnoid, dura mater
|
|
|
Subdural space
|
between dura mater and arachnoid
|
|
|
subarachnoid space
|
between arachnoid and pia mater, filled with CSF
|
|
|
Cognitive functions
|
attention, memory, language, visual and spatial skills, reasoning
|
|
|
two types of cerebrovascular disease
|
cerebral infarction and cerebral hemorrhage
|
|
|
Cerebral infarction
|
caused by ischemia - lack of blood supply due to obstruction due to embolism or thrombosis
|
|
|
What produces neuronal death in cerebral infarction?
|
anoxia and hypoglycemia
|
|
|
Cerebral hemorrhage
|
caused by bleeding due to rupture of aneurysm or traumatic
|
|
|
What causes neuronal death in cerebral hemorrhage
|
blood neurotoxicity and anoxia and hypoglycemia
|
|
|
Embolism
|
traveling object, can be solid - blood clot or fat from fractures, or gas - oxygen, nitrogen, or superficial jugular vein cut
|
|
|
Anterior cerebral artery damage
|
hemorrhage due to aneurysm rupture results in anterograde and retrograde amnesia for more then a week preceedong hemorrhage and confaulation
|
|
|
Anterior communicating artery damage
|
aneurysm trapping produces severe amnesia in 90 % cases, failure to release from proactive interference, confabulation
|
|
|
Middle cerebral artery damage
|
cause - infarction, severe motor and sensory deficits, aphasia (inability to understand language if left artery is involved (80 % cases)), mild memory deficits, recognition memory affected
|
|
|
Posterior cerebral artery damage
|
severe memory deficits (paired associate learning), retrograde amnesia, difficult color identification, cortical blindness, NO CONFABULATION
|
|
|
Mechanism of neuronal cell death by ischemia (necrosis)
|
lack of O2 causes high levels of extracellular glutamate and K due to pump failure, produce depolarization, increases Ca in presynaptic terminal, further increases extracellular glutamate, K, further depolarization, leads to high cytosolic Ca - TRIGGERING CELL DEATH MECHANISM, massive activation of kinases, then calpain and other proteolytic enzymes, cell begins autodigesting. High concentr. of cytosolic Ca evokes secondary rise of cytosolic Ca due Ca induced release from ER, produces subnormal resting intracellular Ca and increased firing rate of neuron, neuronal death causes gliosis - scar tissue
|
|
|
Aneurysm
|
balloning of an artery can be congenital, 5 % of population, ACA MCA most prone
|
|
|
Types of aneurysm
|
saccular - most common type, berry aneurysm (shape), has neck and stem
fusiform - less common, outpouching of an arterial wall on both sides, no stem |
|
|
Memory impairment after aneurysm
|
anterograde amnesia - confabulation
|
|
|
Toxic effect of blood
|
when blood brain barrier disrupted - toxic effect on the brain
|
|
|
Generation of action potentials
|
due to influx/efflux through Na and K voltage dependent channels due to concentration gradient and electrical gradient and through active transporters - pumps, Na K exchange
|
|
|
Consequences of AP
|
Ca influx through VDCCs- signal transduction cascade, liberation of glutamate from presynaptic terminal
|
|
|
Glutamate toxicity
|
lack of oxygen causes glia to release glutamate - Ca influx through NMDA
|
|
|
Causes of necrosis
|
energy depletion, dissipation of ionic gradients, cell swelling, dissipation/permeabilization of plasma membrane, loss of intracellular contents
|
|
|
Consequences of necrosis
|
inflammatory response + gliosis
|
|
|
Alcohols properties
|
CNS depressant, absorbed to blood from small intestine, reduces inhibitions
|
|
|
Stages of alcohol intoxication
|
1. subclinical -normal behavior
2. euphoria - mild euphoria, sociability, decreased inhiitions, less attention 3. Excitement - emotional instability, loss of judgement, drowsiness, impaired balance 4.confusion - disorientation, mental confusion, dizziness, apathy 5.stupor - vomiting incontinence, sleep/stupor 6.coma (0.35-0.50) - subnormal body temperature, impaired circulation and respiration, possible death 0.45+ - death |
|
|
Distriution of alcohol
|
high affinity for water in fluids
|
|
|
Elimination of alcohol
|
through liver metabolism, oxidized alcohol to acetaldehyde to acetic acid to carbon dioxide and water
|
|
|
Neuropharmocology of alcohol
|
ethanol affects different cerebral NT's - GABA, inhibitory NT
|
|
|
ACute alcoholic intoxication
|
interferes with sensory store, especially verbal and visual, depressive effect on recency effect, no retrieval deficits
|
|
|
State dependent learning
|
information is learned by person while intoxicated more completely retrieved in similar state
|
|
|
Wernickes encephalopathy
|
thiamine defficiency, ataxia, ophtalmoplegia, nystagmus + confusional state
|
|
|
Korskoffs amnesia
|
anterograde memory deficits - everyday memory symptoms (unable to recall time and space), confabulation, impaired STM
retrograde memory deficits |
|
|
Anatomical site of lesions
|
thalamus and/or mammilary bodies, nucleus basalis
|
|
|
Pathophysiology of Wernicke Korsakoff
|
consequence of thiamine defficiency, consequence of chronic alcoholism because of the diet
|
|
|
Memory deficits
|
anterograde - severe but incomplete, retrograde more for most recent events, confabulation
|
|
|
symptoms of alcoholism
|
craving, loss of control, tolerance, physical dependence
|
|
|
N.A case
|
penetrating brain injury with miniature fencing foil, lesion of left dorsomedial nucleus of thalamus, severe anterograde amnesia, retrograde amnesia for 2 years prior to accident, normal intelligence, more severe on verbal then non verbal
|
|
|
B. Y case
|
bilateral thalamic lesion, caused by infarction, normal intelligence, no sensory/perceptual deficits, severe retrograde and anterograde amensia, retrograde amnesia improved with time
|
|
|
Dementia
|
intellectual deterioration, affects 4 milliom Americans, 4th major cause of death, caused by degenerative disease of the brain
|
|
|
2 types of dementia
|
1. cortical - little involvement of motor system, preservation of gait, muscle tone, reflex, deterioration of language memory, IQ, aphasia, amnesia, agnosia ex - Alzheimers
2.subcortical - motor system affected, language mildly affected, ex - huntingtons, Parkinsons |
|
|
Neuropathology of Alzheimers
|
neurofibrillary tangles and neuritic plaque, appear earliest in entorhinal cortex and hippocampus (CA1), followed by association cortices of frontal parietal and temporal lobes, neurons most affected - pyramidal shaped neurons of cortical layers
|
|
|
Neurofibrillary tangle formation
|
intracellular, protein tau in microtubules becomes extraphosphoryllated, causes tangles, leads to cell atrophy and death
|
|
|
Amyloid plaques
|
diffuse plaque, amyloid deposits, extracellular
|
|
|
Risk factors for AD
|
increasing age, female sex, environmental factors
|
|
|
Stages of ALzheimers
|
1. Early/mild - memory loss, especially recent events , episodic - names, conversations, personality changes - easily upset, anxious
middle/moderate - worsening memory loss, especially current events, depression, withdrawal, confusion 3. Later/severe- unaware of time/place, cant identify family members,, require constant care |
|
|
Disconection syndrome
|
hippocampus disconects from association cortices
|
|
|
H.M case
|
removal of bilateral medial temporal lobes, anterior 2/3 hippocampus, posthippocampal gyrus, amygdala, total anterograde amnesia, little retrograde, 2-3 years prior to surgery, IQ and perceptual skills normal, social skills personality intact, STM good,
|
|
|
Significance of H.M case
|
first unambiguous case of amnesia produced by lesion, first to demonstrate that medial temporal loe participates in memory ( not emotion), distinction between procedural/declarative memory is biological, animal models on nonhuman primates
|
|
|
R.B case
|
postmortem, amnesia from ischemic episode, died 5 years after, severe anterograde, slight retrograde, aware of condition, bilateral lesion onvolving CA1, highest density of NMDA receptors in brain
|
